Turns out that when the going got tough, Bay’s oysters got tougher
Faced with MSX threat, dermo became more virulent while oysters shifted their spawning to thwart both.
Not long ago, Ryan Carnegie decided to take a look at some old samples of the oyster parasite dermo that had been archived for decades at the Virginia Institute of Marine Science.
What the shellfish pathologist saw when he peered at Perkinsus marinus through the microscope may change the way people look at oyster disease in Chesapeake Bay.
“The first sample I looked at was like, ‘Wow, this is not our Perkinsus,’” Carnegie recalled.
Dermo cells collected from oysters in the 1960s were significantly larger than those found today, and there were fewer parasites.
His conclusions — stemming from a fresh, long-term look at dermo in the Bay, along with work by other scientists at VIMS — are leading to a new theory about the battle for dominance between two competing oyster parasites — a battle that left most of the Bay’s oysters dead as collateral damage.
It’s a theory that involves some highly unpredictable twists. It suggests the native parasite, dermo, “won” the battle against the nonnative parasite, MSX, to become the Bay’s primary oyster parasite — but only after it changed to become much more deadly to the native oyster.
Meanwhile, oysters may be adapting to the disease, at least in Virginia, by reducing their period of spawning — yet increasing reproductive success. That’s a risky strategy, but over the last decade it has resulted in more young oysters “recruiting” into the population, creating a small population rebound from historic lows.
If correct — and not everyone is sure they are — the conclusions suggest that both the diseases, and the oysters, have adapted to changes more abruptly than thought possible — and in ways few would have predicted.
“Who would have ever believed that making the native disease more virulent would have arguably ended up increasing recruitment in the native oyster population?” asked Roger Mann, a longtime oyster researcher at VIMS who, with Carnegie, has been developing the new theory.
Carnegie and Mann caution that their data is drawn mostly from Virginia, and that some of their conclusions may not hold for Maryland, where disease dynamics can be different because of lower-salinity water.
Oysters, and the towering reefs they built, were once one of the most dominant features of the Chesapeake. But overharvesting in the late 1800s and early 1900s destroyed their habitat and reduced their numbers.
By the mid-1900s, they faced the added challenge posed by two parasites.
Dermo has long been present in the lower Chesapeake, where it was originally found at low levels and with low rates of mortality. When dermo killed oysters, it usually took years to do so.
Then, in the 1950s, a parasite from Asia — MSX, or Haplosporidium nelsoni — suddenly emerged. It quickly began killing huge numbers of oysters in Delaware Bay, where it was first detected, and in 1959 it reached the Chesapeake.
In high salinity Virginia waters, where the parasite thrived, it killed more than 90 percent of the oysters on many reefs, and killed them quickly — often within a few months.
Both MSX and dermo like warm water and high salinities, though dermo tolerates lower salinities than MSX. So the disease situation worsened significantly in the mid-1980s when warm, dry years increased salinities and allowed the diseases to reach unaffected areas, including many of Maryland’s reefs.
Oyster populations dropped to less than 1 percent of historic levels. Harvests collapsed. Oysters that once lived 6–8 years struggled to survive the 2–3 years it took to reach the 3-inch market size.
Many watermen, fishery managers and scientists began calling for introducing a nonnative oyster that could withstand the diseases. In meetings, the native oyster was sometimes derided as a “wimp.”
That’s where the change Carnegie saw under the microscope comes in.
Carnegie believes the reason the oyster situation looked so bleak in the Bay was because dermo changed. In the 1960s and ’70s, MSX was the Bay’s primary killer, often killing oysters before dermo could even be detected. But in the 1980s, dermo also became a major killer. “Something happened, fundamentally, for the parasite,” Carnegie said. “It became a much more aggressive and virulent pathogen.”
Scientists at the time thought warmer, saltier conditions allowed dermo to become more virulent. But Carnegie’s new look at the archived dermo samples tells a different story.
The parasite physically changed its appearance at about that time, becoming about a third smaller and much more numerous in samples observed under the microscope.
“Did you ever see this?“ Carnegie asked longtime VIMS oyster pathologist Gene Burreson.
“Whoa,” Burreson responded. “This is not the same thing we see today.”
In fact, pathologists looking at disease samples at the time also noted a change. In re-examining their log entries, Carnegie found they began occasionally adding a question mark when they thought they were seeing dermo — “dermo?”
Carnegie believes dermo not only changed appearance, but formed a new phenotype, or variant, which was more virulent in response to competition from MSX.
He cites several lines of evidence that suggest dermo began behaving differently.
In the 1960s, populations of dermo in Virginia oysters were mainly found in the connective tissue of the oysters and were released into the water when the bivalve died. Infections were limited to nearby oysters.
With the arrival of MSX, most oysters died before large concentrations of dermo could build up and be released. In the 1980s, though, dermo was primarily infecting the oyster’s gut and was therefore more likely to be excreted with feces, allowing parasites to escape quickly and find other hosts.
Since the early 1960s, VIMS scientists have placed uninfected oysters in high-salinity York River water and monitored their infections. In the years shortly after MSX appeared, dermo nearly vanished from those oysters. But in the 1980s, Carnegie said, there was an “explosion” of dermo in the oysters — and infections remain at similar levels of intensity today.
“This is a sledgehammer,” Carnegie said. “After the MSX arrival in the 1950s, dermo has gotten a lot worse.”
Dermo, a parasite that evolved with the native oyster, originally acted the way one would expect: If it killed, it did so slowly. After all, a parasite doesn’t want to kill its host because that threatens the parasite as well.
MSX didn’t co-evolve with the native oyster, which had no defense against it. Oysters died in huge numbers from MSX infections — something that also posed a threat to dermo, which was being outcompeted for oyster hosts.
For dermo, it was a matter of adapt, or vanish from the Bay. The result, Carnegie said, was that MSX forced dermo parasites to select toward a “hyper-virulent native parasite — and one we are continuing to have to live with.”
It’s what he calls “the MSX hangover.” MSX, has largely receded from the Bay as a major killer. Infections mainly turn up in young oysters, or in low-salinity areas — where oysters are not routinely exposed to MSX — when dry conditions allow increased salinities that allow the parasite to move upstream. But dermo remains widespread.
The parasites’ onslaught may have helped produce a more robust oyster. While infection levels of dermo have remained the same since the 1980s, mortality caused by the parasite in Virginia has decreased from about 70 percent to 15–20 percent a year. “There are still high levels of infections, but the oysters are tolerating them better than they were,” Carnegie said.
Chris Dungan, an oyster disease researcher with the Maryland Department of Natural Resources, said Carnegie’s idea ”is certainly credible and plausible, and makes quite an interesting story about how parasites might influence each other’s evolution.”
But Dungan, who also collaborates with Carnegie on oyster disease work in the Bay, said he is less convinced there was a completely new phenotype, noting that some dermo samples taken in Maryland continue to have a larger cell size.
“I’m not sure it is a black and white situation,” Dungan said.
Virginia monitoring data hints that oysters may also be adapting to disease pressure through a significant change in spawning over the last decade. Data compiled by Mann from the James, Piankatank and Great Wicomico rivers show that the mean time for oyster spawning — the time when oysters have released half their larvae — has shifted and is more than 30 days earlier since 2000.
The change has been seen in fall oyster surveys, which increasingly find oyster spat — oysters produced that year — are larger, indicating they’ve had more time to grow. A decade ago, a large spat in the survey was about 25 millimeters. Now, 35–40 mm spat are routine.
“This is an enormous change in a 10-year period,” Mann said. “This is very, very atypical.”
The reason, Mann believes, is dermo. Oysters historically spawned from spring to fall, with some of the largest spawns taking place later in the season. But that’s also the time when dermo infections reach their peak, and several studies show that oysters produce significantly fewer larvae when battling infections.
By breeding earlier, the oysters are producing more offspring. In fact, the amount of larvae produced early in the year today is about the same as was produced by similar size oysters in the early 1900s, Mann said.
Earlier reproduction has another benefit, he said. The oysters are larger the next spring, giving them protection from predators such as blue crabs.
The shift coincides with a period of increased reproductive success and an increasing number of oysters. “It’s been a series of really interesting dominoes,” Mann said. “They are definitely doing something biologically that’s in favor of higher reproduction.”
Condensing the oysters’ spawning period also means they spawn less often. “When I came here in the 1980s, we would record as many as five recruitment events per year in these oysters,” Mann said. “Now, rarely do we see evidence of more than two.”
While that appears to have paid off, Mann said it could be risky over time. Oysters, he said, are reproductive “gamblers” that produce huge amounts of larvae in several spawns in the hope that some will occur when conditions best promote larval survival.
“If these trends continue, one of the worries is that you end up with a very narrow spawning season that doesn’t end up being necessarily optimal when matched with the recruitment season,” he said. “In which case, what you would see is years of high recruitment interspersed with years of no recruitment. You would actually have an increase in recruitment failures.”
(In Maryland, surveys that monitor the time of spawning have only been conducted during the last few years, so there are no data as to whether it has had a similar change.)
Carnegie and Mann said none of their conclusions suggest that oysters are poised to return to former abundances. Cumulative disease mortality, though greatly reduced, remains substantial. And so much of the Bay’s reef habitat has disappeared that many oyster larvae literally have no place to go. Abundant habitat could take many decades, if not centuries, to come back.
But the changes suggest that the native oyster is not so wimpy as many had thought. “What we have come to realize is that these are very resilient creatures, despite the myriad assaults on them,” Carnegie said.
They have survived numerous insults from humans— from overharvesting and wholesale habitat destruction to surmounting the challenges of a human-introduced nonnative parasite. And then, an unexpected challenge from a new, hyper virulent form of a native parasite — one that oysters in other places often were not facing. Rather than disappear, oysters have shown signs of adapting, and, if Carnegie and Mann are right, with amazing speed.
“Oysters are actually doing things,” Mann said. “They are not just dumb rocks that are sitting on the bottom. They are, in fact, doing some interesting things on their own.”